Potential treatment for liver injury through suppression of activated Kupffer cells by PPAR γ

体重约300 g的雌性Sprague道利大鼠给予乙醇过氧化物酶体增殖物激活受体γ（PPARγ）的配体-而对血浆和肝脏脂质过氧化物及血浆内毒素水平无明显影响，吡喹酮对乙醇和LPS诱导的肝脏炎症和坏死也有预防作用Pioghtazone可减弱LPS对TNFα mRNA的诱导作用，但对RXRα mRNA的诱导作用不明显。结果表明，pioghtazone可能通过抑制NFκ B途径抑制TNFα mRNA的表达，从而减轻乙醇和LPS诱导的肝损伤。

Female Sprague Dawley rats weighing about 300g were given ethanod (5g/kg BW) intragastncally, and were injected LPS 24h later.Liver injury was induced in this model.Pioghtazone, the ligand for peroxisome proliferates-activated receptor gamma (PPARγ) prevented increase in plasma AST, ALT,and TNFα levels, but not affected on plasma and hepatic levels of lipid peroxide nor plasma endotoxin level in rats.Pioghtazone also prevented hepatic inflammation and necrosis induced by ethanol and LPS.Ethanol and LPS induction of TNFα mRNA in the liver were blunted by Pioghtazone, however, RXRα mRNA were not affected. PPARγ mRNA levels were suppressed by ethanol and LPS, but recaptured by pioghtazone.These results suggest that pioghtazone may prevent liver injury induced by ethanol and LPS by suppression of TNFα mRNA at least partially through NFκ B pathway.